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Journal articles on the topic 'Mice Effect of temperature on'

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Published: 4 June 2021
Last updated: 28 January 2023

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1

Fischer, Alexander W., Robert I. Csikasz, Gabriella von Essen, Barbara Cannon, and Jan Nedergaard. "No insulating effect of obesity." American Journal of Physiology-Endocrinology and Metabolism 311, no. 1 (July 1, 2016): E202—E213. http://dx.doi.org/10.1152/ajpendo.00093.2016.

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The development of obesity may be aggravated if obesity itself insulates against heat loss and thus diminishes the amount of food burnt for body temperature control. This would be particularly important under normal laboratory conditions where mice experience a chronic cold stress (at ≈20°C). We used Scholander plots (energy expenditure plotted against ambient temperature) to examine the insulation (thermal conductance) of mice, defined as the inverse of the slope of the Scholander curve at subthermoneutral temperatures. We verified the method by demonstrating that shaved mice possessed only half the insulation of nonshaved mice. We examined a series of obesity models [mice fed high-fat diets and kept at different temperatures, classical diet-induced obese mice, ob/ob mice, and obesity-prone (C57BL/6) vs. obesity-resistant (129S) mice]. We found that neither acclimation temperature nor any kind or degree of obesity affected the thermal insulation of the mice when analyzed at the whole mouse level or as energy expenditure per lean weight. Calculation per body weight erroneously implied increased insulation in obese mice. We conclude that, in contrast to what would be expected, obesity of any kind does not increase thermal insulation in mice, and therefore, it does not in itself aggravate the development of obesity. It may be discussed as to what degree of effect excess adipose tissue has on insulation in humans and especially whether significant metabolic effects are associated with insulation in humans.
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2

Kluger, M. J., C. A. Conn, B. Franklin, R. Freter, and G. D. Abrams. "Effect of gastrointestinal flora on body temperature of rats and mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 2 (February 1, 1990): R552—R557. http://dx.doi.org/10.1152/ajpregu.1990.258.2.r552.

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The purpose of these experiments was to test the hypothesis that gut flora influences the body temperature of rodents. Rats and mice were implanted with biotelemetry transmitters that enabled us to record both abdominal temperature and activity for long periods of time. Rats given nonabsorbable antibiotics in their drinking water, which reduced their gut flora, had a marked decrease in both their daytime and nighttime temperatures. Similar results were found with germfree mice. The circadian rhythms in body temperature of germfree and conventionalized mice were not different. However, the body temperatures of the germfree mice were lower than those of the conventionalized mice during both the daytime and nighttime. The decrease in body temperature in the germfree mice was not related to changes in activity. These results support the hypothesis that gut flora has a tonic stimulatory effect on both the daytime and nighttime body temperature of rodents.
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3

Miyazaki, S., F. Ishikawa, S. Matsuo, and K. Yamaguchi. "Effect of fluoroquinolones on body temperature of mice." Journal of Antimicrobial Chemotherapy 62, no. 6 (September 10, 2008): 1319–22. http://dx.doi.org/10.1093/jac/dkn418.

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4

Hishimura, Yutaka, and Kana Itoh. "Effect of social interaction on skin temperature in mice." Japanese journal of psychology 80, no. 2 (2009): 152–58. http://dx.doi.org/10.4992/jjpsy.80.152.

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5

Vargas, M. L., F. Tejada, A. Peñuela, R. Peñafiel, and A. Cremades. "Effect of potassium deficiency on body temperature in mice." Journal of Thermal Biology 25, no. 1-2 (February 2000): 125–29. http://dx.doi.org/10.1016/s0306-4565(99)00089-3.

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6

Izumizaki, Masahiko, Michiko Iwase, Hiroshi Kimura, Takayuki Kuriyama, and Ikuo Homma. "Central histamine contributed to temperature-induced polypnea in mice." Journal of Applied Physiology 89, no. 2 (August 1, 2000): 770–76. http://dx.doi.org/10.1152/jappl.2000.89.2.770.

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Breathing pattern is influenced by body temperature. However, the central mechanism for changing breathing patterns is unknown. Central histamine is involved in heat loss mechanisms in behavioral studies, but little is known about its effect on breathing patterns. We examined first the effect of body temperature on breathing patterns with increasing hypercapnia in conscious mice and then that of the depletion of central histamine by S(+)-α-fluoromethylhistidine hydrochloride (α-FMH) (100 mg/kg ip), a specific inhibitor of histidine decarboxylase, at normal and raised body temperatures. A raised body temperature increased respiratory frequency with reductions in both inspiratory and expiratory time and decreased tidal volume. On the other hand, α-FMH lowered respiratory frequency with a prolongation of expiratory time at the raised temperature; however, this was not observed at a normal temperature. These results indicate that central histamine contributes to an increase in respiratory frequency as a result of a reduction in expiratory time when body temperature is raised.
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7

Gatti, Silvia, Jennifer Beck, Giamila Fantuzzi, Tamas Bartfai, and Charles A. Dinarello. "Effect of interleukin-18 on mouse core body temperature." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 3 (March 1, 2002): R702—R709. http://dx.doi.org/10.1152/ajpregu.00393.2001.

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We have studied, using a telemetry system, the pyrogenic properties of recombinant murine interleukin-18 (rmIL-18) injected into the peritoneum of C57BL/6 mice. The effect of IL-18 was compared with the febrile response induced by human IL-1β, lipopolysaccharide (LPS), and recombinant murine interferon-γ (rmIFN-γ). Both IL-1β and LPS induced a febrile response within the first hour after the intraperitoneal injection, whereas rmIL-18 (10–200 μg/kg) and rmIFN-γ (10–150 μg/kg) did not cause significant changes in the core body temperature of mice. Surprisingly, increasing doses of IL-18, injected intraperitoneally 30 min before IL-1β, significantly reduced the IL-1β-induced fever response. In contrast, the same pretreatment with IL-18 did not modify the febrile response induced by LPS. IFN-γ does not seem to play a role in the IL-18-mediated attenuation of IL-1β-induced fever. In fact, there was no elevation of IFN-γ in the serum of mice treated with IL-18, and a pretreatment with IFN-γ did not modify the fever response induced by IL-1β. We conclude that IL-18 is not pyrogenic when injected intraperitoneally in C57BL/6 mice. Furthermore, a pretreatment with IL-18, 30 min before IL-1β, attenuates the febrile response induced by IL-1β.
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8

Hassan, Intisar A., Zachary Renfro, Harrison Blake, Satyajit Rath, and Jeannine M. Durdik. "Effect of temperature on functional activity of macrophages in three different species." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 149.17. http://dx.doi.org/10.4049/jimmunol.204.supp.149.17.

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Abstract Temperature affects body physiological functions, including immunity in ways that influence survival. This study investigated the effect of temperature on macrophage activation and metabolism across species. Macrophages were isolated from mice, chicken or rainbow trout primary tissue or from macrophage cell lines and were activated with lipopolysaccharide (LPS) or IFN-γ. For mice, both Raw264.7 and primary cells, nitric oxide (NO) production was similar at 35°C and 37°C but dropped dramatically at temperatures below 35°C. At fever temperature (39°C), NO release increased in response to LPS. Young bone marrow derived macrophage (BMDM) and peritoneal resident macrophage (PRM) showed increased protein synthesis at 39°C compared to 37°C. Chicken splenic macrophages (CSM) showed NO responses that were similar at 37, 39, and at 41°C (normal for avian). A fever of 42°C had a large stimulatory effect on NO production compared to 41°C. A chicken liver derived macrophage cell line, HTC, showed the same pattern. They also showed higher protein synthesis at 42°C compared with (41°C) after LPS stimulation. Trout head-kidney macrophages (THM) showed the highest NO responses at 19°C when compared to more typical stream temperatures of 13, 15, and 16°C. They still showed some response at 28 and 37°C. Thus, their macrophages respond at higher temperatures than the fish can tolerate. Stimulated THM cells with LPS at 19°C showed increased protein synthesis compared to 13 and 16°C. We can conclude from our experiments that fish macrophages had a much broader range of temperatures at which they could respond by NO generation and protein synthesis compared to mice and chickens and all had increased responses at fever temperatures.
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9

Small, Lewin, Henry Gong, Christian Yassmin, Gregory J. Cooney, and Amanda E. Brandon. "Thermoneutral housing does not influence fat mass or glucose homeostasis in C57BL/6 mice." Journal of Endocrinology 239, no. 3 (December 2018): 313–24. http://dx.doi.org/10.1530/joe-18-0279.

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One major factor affecting physiology often overlooked when comparing data from animal models and humans is the effect of ambient temperature. The majority of rodent housing is maintained at ~22°C, the thermoneutral temperature for lightly clothed humans. However, mice have a much higher thermoneutral temperature of ~30°C, consequently data collected at 22°C in mice could be influenced by animals being exposed to a chronic cold stress. The aim of this study was to investigate the effect of housing temperature on glucose homeostasis and energy metabolism of mice fed normal chow or a high-fat, obesogenic diet (HFD). Male C57BL/6J(Arc) mice were housed at standard temperature (22°C) or at thermoneutrality (29°C) and fed either chow or a 60% HFD for 13 weeks. The HFD increased fat mass and produced glucose intolerance as expected but this was not exacerbated in mice housed at thermoneutrality. Changing the ambient temperature, however, did alter energy expenditure, food intake, lipid content and glucose metabolism in skeletal muscle, liver and brown adipose tissue. Collectively, these findings demonstrate that mice regulate energy balance at different housing temperatures to maintain whole-body glucose tolerance and adiposity irrespective of the diet. Despite this, metabolic differences in individual tissues were apparent. In conclusion, dietary intervention in mice has a greater impact on adiposity and glucose metabolism than housing temperature although temperature is still a significant factor in regulating metabolic parameters in individual tissues.
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10

Konecka, Anna Maria, Irmina Sroczynska, and Andrzej W. Lipkowski. "The effect of enkephalin dimers on body temperature in mice." Peptides 8, no. 3 (May 1987): 431–35. http://dx.doi.org/10.1016/0196-9781(87)90005-2.

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11

O'Connor, C. S., L. I. Crawshaw, A. Kosobud, R. C. Bedichek, and J. C. Crabbe. "The effect of ethanol on behavioral temperature regulation in mice." Pharmacology Biochemistry and Behavior 33, no. 2 (June 1989): 315–19. http://dx.doi.org/10.1016/0091-3057(89)90506-6.

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12

Catalina, Fernando, Leon Milewich, William Frawley, Vinay Kumar, and Michael Bennett. "Decrease of Core Body Temperature in Mice by Dehydroepiandrosterone." Experimental Biology and Medicine 227, no. 6 (June 2002): 382–88. http://dx.doi.org/10.1177/153537020222700603.

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Dietary dehydroepiandrosterone (DHEA) reduces food intake in mice, and this response is under genetic control. Moreover, both food restriction and DHEA can prevent or ameliorate certain diseases and mediate other biological effects. Mice fed DHEA (0.45% w/w of food) and mice pair-fed to these mice (food restricted) for 8 weeks were tested for changes in body temperature. DHEA was more efficient than food restriction alone in causing hypothermia. DHEA injected intraperitoneally also induced hypothermia that reached a nadir at 1 to 2 hr, and slowly recovered by 20 to 24 hr. This effect was dose dependent (0.5–50 mg). Each mouse strain tested (four) was susceptible to this effect, suggesting that the genetics differ for induction of hypophagia and induction of hypothermia. Because serotonin and dopamine can regulate (decrease) body temperature, we treated mice with haloperidol (dopamine receptor antagonist), 5,7-dihydroxytryptamine (serotonin production inhibitor), or ritanserin (serotonin receptor antagonist) prior to injection of DHEA. All of these agents increased rather than decreased the hypothermic effects of DHEA. DHEA metabolites that are proximate (5-androstene-3β, 17β-diol and androstenedione) or further downstream (estradiol-17β) were much less effective than DHEA in inducing hypothermia. However, the DHEA analog, 16α-chloroepiandrosterone, was as active as DHEA. Thus, DHEA administered parentally seems to act directly on temperature-regulating sites in the body. These results suggest that DHEA induces hypothermia independent of its ability to cause food restriction, to affect serotonin or dopamine functions, or to act via its downstream steroid metabolites.
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13

Zhou, Wei, Ruxue Lei, Chuanyi Zuo, Yunqing Yue, Qin Luo, Chengshun Zhang, Peng Lv, Yong Tang, Haiyan Yin, and Shuguang Yu. "Analgesic Effect of Moxibustion with Different Temperature on Inflammatory and Neuropathic Pain Mice: A Comparative Study." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/4373182.

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The aim of this study was to determine whether variation of temperature during moxibustion would generate division of analgesic effect. The moxibustion with different temperatures (37°C, 42°C, 47°C, and 52°C) was applied to ST36 acupoint for 30 minutes in chronic inflammatory or neuropathic pain mice. The analgesic effect was evaluated by thermal hyperalgesia test in chronic inflammatory pain and by mechanical allodynia in neuropathic pain, respectively. The results indicated that interventions of moxibustion with different temperature caused different analgesic effect on either chronic inflammatory induced by injection of complete Freund’s adjuvant (CFA) or neuropathic pain induced by spared nerve injury (SNI). In chronic inflammatory pain, different moxibustion temperature generated different intensity of analgesic effect: the higher the better. In chronic neuropathic pain, stronger analgesic effect was found in moxibustion with temperature 47°C or 52°C other than 37°C and 42°C. However, there is no significant difference displayed between moxibustion temperatures 47°C and 52°C or 37°C and 42°C. It implies that the temperature should be taken into account for moxibustion treatment to chronic inflammatory or neuropathic pain.
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14

Lewis, G. B. H. "Effect of Altered Environmental Temperature on Established Infection." Anaesthesia and Intensive Care 16, no. 3 (August 1988): 338–41. http://dx.doi.org/10.1177/0310057x8801600316.

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An alteration of ten degrees Celsius in environmental temperature significantly alters the mortality from severe established Escherichia coli and Staphylococcus aureus infection in mice. Many patients with severe infection are nursed in wards without air conditioning. It is suggested that even modest levels of environmental stress may influence their recovery.
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15

Chen, Minhui, Guanxi Qiao, Bonnie L. Hylander, Hemn Mohammadpour, Anurag K. Singh, and Elizabeth A. Repasky. "Mandated Cool Housing Temperature and Adrenergic Stress reduce the efficacy of radiation and mask the “Abscopal Effect” in mouse models of cancer." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 136.27. http://dx.doi.org/10.4049/jimmunol.202.supp.136.27.

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Abstract Mice used for modeling cancer and anti-tumor immunity experience increased adrenergic stress due to IACUC-mandated cool housing temperatures. We wondered if this source of stress could be impacting the efficacy of ionizing radiation and the frequency of an “abscopal” effect (in which tumors outside the field of irradiation exhibit a response, an effect linked to enhanced systemic anti-tumor immunity). When mice bearing two separate CT26 tumors were housed at a thermoneutral temperature (TT; ~30°C) and 6 Gy of radiation was delivered to one tumor, control of both the irradiated and non-irradiated tumors was much greater than that seen in both tumors of mice housed at standard cool temperature (ST; ~22°C). Moreover, when tumor bearing mice housed at ST were treated with the pan β-blocker, propranolol and radiation, we observed a significantly improved growth control of irradiated and non-irradiated tumors. These effects were lost in SCID mice, and in mice depleted of CD8+T-cells. Experiments using knockout mice specifically identified a role for the β2 adrenergic receptor in mediating these effects. Moreover, we found that intra-tumoral effector T-cells, including IFN-γ+, GzmB+, TNFα+ and T-bet+CD8+T-cells, as well as the ratio of IFNγ+CD8+T-cells to Tregs, increased while numbers of MDSC and Tregs decreased, in mice treated with β-blocker and radiation. Finally, cured mice treated with propranolol and radiation rejected local and distant rechallenges in a tumor-specific manner. In conclusion, these data suggest that adrenergic stress plays a major role in regulating the efficacy of radiation therapy. Blockade of β2 adrenergic signaling could be a useful new strategy in the radiation oncology clinic.
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16

Conn, C. A., B. Franklin, R. Freter, and M. J. Kluger. "Role of gram-negative and gram-positive gastrointestinal flora in temperature regulation of mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 6 (December 1, 1991): R1358—R1363. http://dx.doi.org/10.1152/ajpregu.1991.261.6.r1358.

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An earlier study showed that the presence of gut flora elevates body temperature of mice and rats. In these experiments, we questioned whether the signal coming from the gut was endotoxin from gram-negative (Gm-) bacteria or some signal derived from gram-positive (Gm+) microorganisms. To test the idea that endotoxin is responsible for the effects of flora, we compared the temperature of the endotoxin-resistant mouse (C3H/HeJ) with that of endotoxin-sensitive strains of mice (C3H/SnJ and C3H/HeN). Temperature of C3H/HeJ was not different from that of C3H/SnJ or C3H/HeN during the light period but was significantly lower during the later hours of the dark period. We speculated that, if endotoxin leaking across the gut wall were responsible for elevating temperature, then reduction of gut flora with nonabsorbable antibiotics would depress the temperature of the endotoxin-sensitive mice more than that of the endotoxin-resistant mice. Because antibiotics lowered the temperature of both strains of mice to the same extent, the signal coming from the gut is unlikely to be endotoxin. To test whether Gm+ flora can be responsible for elevating temperature, we inoculated one group of germfree mice with Gm+ organisms. Their mean temperature was significantly higher than that of mice that remained germfree. Cecectomy had no effect on temperature, indicating that the special properties of the germfree cecum were not involved in lowering the temperature of germfree mice. These data support the hypotheses that Gm+ organisms are a major source of the stimulatory effect of flora on normal body temperature and that the presence of Gm- organisms is unnecessary.
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17

Swoap, Steven J., J. Michael Overton, and Graham Garber. "Effect of ambient temperature on cardiovascular parameters in rats and mice: a comparative approach." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 2 (August 2004): R391—R396. http://dx.doi.org/10.1152/ajpregu.00731.2003.

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Ambient air temperatures (Ta) of <6°C or >29°C have been shown to induce large changes in arterial blood pressure and heart rate in homeotherms. The present study was designed to investigate whether small incremental changes in Ta, such as those found in typical laboratory settings, would have an impact on blood pressure and other cardiovascular parameters in mice and rats. We predicted that small decreases in Ta would impact the cardiovascular parameters of mice more than rats due to the increased thermogenic demands resulting from a greater surface area-to-volume ratio in mice relative to rats. Cardiovascular parameters were measured with radiotelemetry in mice and rats that were housed in temperature-controlled environments. The animals were exposed to different Ta every 72 h, beginning at 30°C and incrementally decreasing by 4°C at each time interval to 18°C and then incrementally increasing back up to 30°C. As Ta decreased, mean blood pressure, heart rate, and pulse pressure increased significantly for both mice (1.6 mmHg/°C, 14.4 beats·min−1·°C−1, and 0.8 mmHg/°C, respectively) and rats (1.2 mmHg/°C, 8.1 beats·min−1·°C−1, and 0.8 mmHg/°C, respectively). Thus small changes in Ta significantly impact the cardiovascular parameters of both rats and mice, with mice demonstrating a greater sensitivity to these Ta changes.
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18

Richard, D., A. Labrie, and S. Rivest. "Tissue specificity of SNS response to exercise in mice exposed to low temperatures." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, no. 5 (May 1, 1992): R921—R925. http://dx.doi.org/10.1152/ajpregu.1992.262.5.r921.

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The present study was carried out to investigate the tissue specificity of the sympathetic nervous system (SNS) response to acute exercise in adult mice exposed to four ambient temperatures. SNS activity estimates in heart, pancreas, and brown adipose tissue (BAT) were obtained from the measurement of the dopamine (DA) tissue contents 1 h after the inhibition of the DA-beta-hydroxylase with 1-cyclohexyl-2-mercaptoimidazole (CHMI). DA was measured by electrochemical detection after the separation of the monoamine using high-performance liquid chromatography. In both heart and pancreas, temperature and activity influenced DA tissue contents after the CHMI injection. In these tissues, and regardless of whether mice were resting or exercising, the DA contents gradually increased while the ambient temperature was dropped from a thermoneutral temperature of 32 to 5 degrees C. In BAT, however, there was a significant interaction between temperature and activity on the tissue DA content; in contrast to what was observed in resting animals, DA did not uniformly augment in exercising mice when the temperature was decreased from 32 to 5 degrees C. In summary, the present results show that exercise can attenuate the stimulating effect of cold on SNS activity in BAT. This effect is seemingly specific to BAT because, in mice exposed to low ambient temperatures, SNS activity in both heart and pancreas is not lower in exercising than in resting animals.
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19

Wernstedt, Ingrid, Amanda Edgley, Anna Berndtsson, Jenny Fäldt, Göran Bergström, Ville Wallenius, and John-Olov Jansson. "Reduced stress- and cold-induced increase in energy expenditure in interleukin-6-deficient mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 3 (September 2006): R551—R557. http://dx.doi.org/10.1152/ajpregu.00514.2005.

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Interleukin-6 (IL-6) deficient (-/-) mice develop mature onset obesity. Pharmacological studies have shown that IL-6 has direct lipolytic effects and when administered centrally increases sympathetic outflow. However, the metabolic functions of endogenous IL-6 are not fully elucidated. We aimed to investigate the effect of IL-6 deficiency with respect to cold exposure and cage-switch stress, that is, situations that normally increase sympathetic outflow. Energy metabolism, core temperature, heart rate, and activity were investigated in young preobese IL-6−/− mice by indirect calorimetry together with telemetry. Baseline measurements and the effect of cage-switch stress were investigated at thermoneutrality (30°C) and at room temperature (20°C). The effect of cold exposure was investigated at 4°C. At 30°C, the basal core temperature was 0.6 ± 0.24°C lower in IL-6−/− compared with wild-type mice, whereas the oxygen consumption did not differ significantly. The respiratory exchange ratio at 20°C was significantly higher and the calculated fat utilization rate was lower in IL-6−/− mice. In response to cage-switch stress, the increase in oxygen consumption at both 30 and 20°C was lower in IL-6−/− than in wild-type mice. The increase in heart rate was lower in IL-6−/− mice at 30°C. At 4°C, both the oxygen consumption and core temperature were lower in IL-6−/− compared with wild-type mice, suggesting a lower cold-induced thermogenesis in IL-6−/− mice. The present results indicate that endogenous IL-6 is of importance for stress- and cold-induced energy expenditure in mice.
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20

Kolbe, Thomas, Caroline Lassnig, Andrea Poelzl, Rupert Palme, Kerstin E. Auer, and Thomas Rülicke. "Effect of Different Ambient Temperatures on Reproductive Outcome and Stress Level of Lactating Females in Two Mouse Strains." Animals 12, no. 16 (August 20, 2022): 2141. http://dx.doi.org/10.3390/ani12162141.

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Ambient temperature is an important non-biotic environmental factor influencing immunological and oncological parameters in laboratory mice. It is under discussion which temperature is more appropriate and whether the commonly used room temperature in rodent facilities of about 21 °C represents a chronic cold stress or the 30 °C of the thermoneutral zone constitutes heat stress for the animals. In this study, we selected the physiological challenging period of lactation to investigate the influence of a cage temperature of 20 °C, 25 °C, and 30 °C, respectively, on reproductive performance and stress hormone levels in two frequently used mouse strains. We found that B6D2F1 hybrid mothers weaned more pups compared to C57BL/6N mothers, and that the number of weaned pups was reduced when mothers of both strains were kept at 30 °C. Furthermore, at 30 °C, mothers and pups showed reduced body weight at weaning and offspring had longer tails. Despite pronounced temperature effects on reproductive parameters, we did not find any temperature effects on adrenocortical activity in breeding and control mice. Independent of the ambient temperature, however, we found that females raising pups showed elevated levels of faecal corticosterone metabolites (FCMs) compared to controls. Peak levels of stress hormone metabolites were measured around birth and during the third week of lactation. Our results provide no evidence of an advantage for keeping lactating mice in ambient temperatures near the thermoneutral zone. In contrast, we found that a 30 °C cage temperature during lactation reduced body mass in females and their offspring and declined female reproductive performance.
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21

Serrat, Maria A., Rebecca M. Williams, and Cornelia E. Farnum. "Exercise mitigates the stunting effect of cold temperature on limb elongation in mice by increasing solute delivery to the growth plate." Journal of Applied Physiology 109, no. 6 (December 2010): 1869–79. http://dx.doi.org/10.1152/japplphysiol.01022.2010.

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Ambient temperature and physical activity modulate bone elongation in mammals, but mechanisms underlying this plasticity are a century-old enigma. Longitudinal bone growth occurs in cartilaginous plates, which receive nutritional support via delivery of solutes from the vasculature. We tested the hypothesis that chronic exercise and warm temperature promote bone lengthening by increasing solute delivery to the growth plate, measured in real time using in vivo multiphoton microscopy. We housed 68 weanling female mice at cold (16°C) or warm (25°C) temperatures and allowed some groups voluntary access to a running wheel. We show that exercise mitigates the stunting effect of cold temperature on limb elongation after 11 days of wheel running. All runners had significantly lengthened limbs, regardless of temperature, while nonrunning mice had shorter limbs that correlated with housing temperature. Tail length was impacted only by temperature, indicating that the exercise effect was localized to limb bones and was not a systemic endocrine reaction. In vivo multiphoton imaging of fluoresceinated tracers revealed enhanced solute delivery to tibial growth plates in wheel-running mice, measured under anesthesia at rest. There was a minimal effect of rearing temperature on solute delivery when measured at an intermediate room temperature (20°C), suggesting that a lasting increase in solute delivery is an important factor in exercise-mediated limb lengthening but may not play a role in temperature-mediated limb lengthening. These results are relevant to the study of skeletal evolution in mammals from varying environments and have the potential to fundamentally advance our understanding of bone elongation processes.
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22

Gordon, C. J., and L. Fogelson. "Comparative effects of hypoxia on behavioral thermoregulation in rats, hamsters, and mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 260, no. 1 (January 1, 1991): R120—R125. http://dx.doi.org/10.1152/ajpregu.1991.260.1.r120.

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Recent studies using reptiles and other ectothermic species have shown that hypoxia lowers the set point for the control of body temperature. This is characterized by a preference for cooler ambient (Ta) and deep body temperatures (Tb) when placed in a temperature gradient. To elucidate the presence of this effect in mammals, the selected Ta and Tb of three rodent species (mouse, hamster, and rat) were measured while subjected to graded hypoxia in a temperature gradient. Individual animals were placed in the gradient for 30 min. Oxygen content of air entering the gradient was then reduced to a constant level for a period of 60 min by dilution with nitrogen. Tb was significantly reduced in all species at %O2 levels of 5.5-10%. Selected Ta was significantly reduced in the mouse at %O2 levels of 5.5 and 7.3%. Selected Ta of the hamster and rat were reduced slightly at %O2 levels of 5.8 and 7.4%, respectively; however, the effect was not statistically significant. To clarify the effects of hypoxia in these two species, the sample size of rat and hamster was increased to strengthen statistical analysis, and the animals were exposed for 60 min to %O2 levels of 7.4 and 6.7%, respectively. Both species exhibited a significant reduction in selected Ta during hypoxia concomitant with hypothermia. These data support the hypothesis that hypoxia lowers the set point for the control of body temperature in rodents.
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23

Waage, A., and T. Espevik. "Interleukin 1 potentiates the lethal effect of tumor necrosis factor alpha/cachectin in mice." Journal of Experimental Medicine 167, no. 6 (June 1, 1988): 1987–92. http://dx.doi.org/10.1084/jem.167.6.1987.

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Human rIL-1 alpha and human rIL-1 beta were examined for their ability to potentiate the lethal and hypothermic effects of mouse rTNF-alpha in mice. The LD50 of rTNF-alpha was 1.5 micrograms/mouse, whereas the LD50 of rTNF-alpha was reduced to 0.4 micrograms/mouse and 0.5 micrograms/mouse when rTNF-alpha was administered in combination with a nonlethal dose of rIL-1 alpha or rIL-1 beta, respectively. A similar rTNF-alpha enhancing effect of the rIL-1 was observed on the temperature response. The results show that the rIL-1 markedly potentiate the effects of rTNF-alpha on lethality and temperature in mice, and support our suggestion that TNF-alpha and IL-1 may have synergistic lethal effect in human septic shock.
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Sosin, Denis Vladimirovich, Andrey Viktorovich Yevseyev, Edgar Andreyevich Parfenov, Vitaliy Andreyevich Pravdivtsev, Marina Anatolyevna Yevseyeva, and Petr Dmitriyevich Shabanov. "HYPOTHERMIC EFFECT OF ANTIHYPOXANTS πQ1983 AND πQ2170." Reviews on Clinical Pharmacology and Drug Therapy 10, no. 4 (December 15, 2012): 78–82. http://dx.doi.org/10.17816/rcf10478-82.

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In experiments on mice the influence of the new antihypoxants (selenium containing metal complex substances πQ1983, πQ2170) on rectal temperature level dynamic after parenteral and enteral introductions was studied. It is established that both substances perform clear dose-dependent hypothermic effect exceeding an action of the antihypoxant amthizole. Was supposed that substance πQ2170 has high acute toxicity affirmed by significant mice death-rate.
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Russell, Lauren N., William S. Hyatt, Brenda M. Gannon, Christy M. Simecka, Mildred M. Randolph, and William E. Fantegrossi. "Effects of Laboratory Housing Conditions on Core Temperature and Locomotor Activity in Mice." Journal of the American Association for Laboratory Animal Science 60, no. 3 (May 1, 2021): 272–80. http://dx.doi.org/10.30802/aalas-jaalas-20-000093.

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Drug developers worldwide assess compound safety and efficacy using measures that include mouse core temperature and locomotor activity. Subtle differences in animal housing conditions between institutions can alter these values, impacting scientific rigor and reproducibility. In these studies, adult male NIH Swiss mice were surgically implanted with radiotelemetry probes that simultaneously monitored core temperature and locomotor activity across various housing conditions. In the first study, ambient temperature was varied between 20 °C and 28°C in groups of singly housed mice. Additional studies held the mice at a constant ambient temperature and examined the effects of cage density (housing animals singly or in groups of 3 or 6), bedding change and provision of nesting material, and the availability of a running wheel on core temperature and locomotor activity. Mice overwhelmingly maintained species-typical core temperatures across all ambient temperatures, across all housing conditions, when bedding was fresh or old, and with or without the provision of cotton squares as nesting material. However, engaging in wheel running and the combination of fresh bedding and cotton squares transiently increased core temperatures beyond the species-typical range. Similarly, the circadian distribution of locomotor activity was significantly disrupted by placing animals in cages with fresh bedding or nesting material, or by performing both of these manipulations concurrently during the light period. These findings suggest that standard husbandry practices and common housing conditions may transiently affect core temperature in adult mice. Furthermore, these practices may have profound and relatively long-lasting effects on motor activity and the regulation of circadian rhythms.
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Endo, Toyoshi, and Tetsuro Kobayashi. "Thyroid-stimulating hormone receptor in brown adipose tissue is involved in the regulation of thermogenesis." American Journal of Physiology-Endocrinology and Metabolism 295, no. 2 (August 2008): E514—E518. http://dx.doi.org/10.1152/ajpendo.90433.2008.

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C.RF- Tshrhyt/hyt mice have a mutated thyroid-stimulating hormone receptor (TSHR), and, without thyroid hormone supplementation, these mice develop severe hypothyroidism. When hypothyroid Tshrhyt/hyt mice were exposed to cold (4°C), rectal temperature rapidly dropped to 23.9 ± 0.40°C at 90 min, whereas the wild-type mice temperatures were 37.0 ± 0.15°C. When we carried out functional rat TSHR gene transfer in the brown adipose tissues by plasmid injection combined with electroporation, there was no effect on the serum levels of thyroxine, although rectal temperature of the mice transfected with pcDNA3.1/Zeo-rat TSHR 90 min after cold exposure remained at 34.6 ± 0.34°C, which was significantly higher than that of Tshrhyt/hyt mice. Transfection of TSHR cDNA increased mRNA and protein levels of uncoupling protein-1 (UCP-1) in brown adipose tissues, and the weight ratio of brown adipose tissue to overall body weight also increased. Exogenous thyroid hormone supplementation to Tshrhyt/hyt mice restored rectal temperature 90 min after exposure to cold (36.8 ± 0.10°C). These results indicate that not only thyroid hormone but also thyroid-stimulating hormone (TSH)/TSHR are involved in the expression mechanism of UCP-1 in mouse brown adipose tissue. TSH stimulates thermogenesis and functions to protect a further decrease in body temperature in the hypothyroid state.
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Dobrea, George M., and Cecilie Goodrich. "Pirenperone effects on temperature preference and body temperature in maturing mice." Physiology & Behavior 39, no. 3 (January 1987): 327–31. http://dx.doi.org/10.1016/0031-9384(87)90230-7.

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28

Wang, Gui-Ying, Ling-Ling Wang, Bin Xu, Jian-Bin Zhang, and Jin-Feng Jiang. "Effects of Moxibustion Temperature on Blood Cholesterol Level in a Mice Model of Acute Hyperlipidemia: Role of TRPV1." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/871704.

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Objectives. To compare the effects of moxibustion at two different temperatures (38°C and 46°C) on the blood cholesterol level in a mice model of acute hyperlipidemia, to detect the different expression levels of transient receptor potential vanilloid subfamily 1 (TRPV1) in the dorsal root ganglions of the wild mice, and to explore the correlation between TRPV1 and moxibustion’s cholesterol-lowering effects.Method. Two different mice models were used: C57BL/6J wild type (WT) and TRPV1 gene knockout (TRPV1−/−). Each model was randomly divided into control group and model group with three subgroups after acute hyperlipidemia was established: model control group, 38°C moxibustion group, and 46°C moxibustion group. The mice in 38°C group and 46°C group were subject to moxibustion. After the therapy, the cholesterol concentration in serum was measured, and the expression of TRPV1 was quantified.Results. In WT mice, moxibustion caused a decrease in blood cholesterol level and upregulation of TRPV1 at the mRNA level, which was significantly greater in the 46°C group. In contrast, in TRPV1−/− mice, the differences of cholesterol-lowering effects of moxibustion were lost.Conclusions. Temperature is one of the important factors affecting the effects of moxibustion, and the cholesterol -lowering effect of moxibustion is related to the activation of TRPV1.
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Bidon, J. C., O. Souilem, M. Gogny, M. Blin, A. Tuan Vu, and A. Jondet. "Effect of temperature reduction on the vas deferens hyperresponsiveness of sensitized mice." Journal of Autonomic Pharmacology 15, no. 4 (August 1995): 227–38. http://dx.doi.org/10.1111/j.1474-8673.1995.tb00307.x.

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Tenchov, Boris, Silviya Abarova, Rumiana Koynova, Lubomir Traikov, and Lyubka Tancheva. "Low-temperature exothermic transitions in brain proteome of mice, effect of scopolamine." Thermochimica Acta 650 (April 2017): 26–32. http://dx.doi.org/10.1016/j.tca.2017.01.012.

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31

Binda, Maria Mercedes, Carlos Roger Molinas, Paul Hansen, and Philippe Robert Koninckx. "Effect of desiccation and temperature during laparoscopy on adhesion formation in mice." Fertility and Sterility 86, no. 1 (July 2006): 166–75. http://dx.doi.org/10.1016/j.fertnstert.2005.11.079.

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Huebert, Terry, William S. Evans, and Marianne Hardy. "Hymenolepis diminuta: The effect of cold temperature exposure on infections in mice." Experimental Parasitology 70, no. 4 (May 1990): 398–403. http://dx.doi.org/10.1016/0014-4894(90)90123-t.

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Berezkin, M. V., V. F. Kudinova, A. N. Batygov, L. E. Ponomareva, and G. N. Zhukova. "Effect of lighting conditions on circadian rhythm of rectal temperature in mice." Bulletin of Experimental Biology and Medicine 106, no. 3 (September 1988): 1337–40. http://dx.doi.org/10.1007/bf00834513.

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34

Rabearivony, Anjara, Huan Li, Shiyao Zhang, Siyu Chen, Xiaofei An, and Chang Liu. "Housing temperature affects the circadian rhythm of hepatic metabolism and clock genes." Journal of Endocrinology 247, no. 2 (November 2020): 183–95. http://dx.doi.org/10.1530/joe-20-0100.

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Environmental temperature remarkably impacts on metabolic homeostasis, raising a serious concern about the optimum housing temperature for translational studies. Recent studies suggested that mice should be housed slightly below their thermoneutral temperature (26°C). On the other hand, the external temperature, also known as a zeitgeber, can reset the circadian rhythm. However, whether housing temperature affects the circadian oscillators of the liver remains unknown. Therefore, we have compared the effect of two housing temperatures, namely 21°C (conventional; TC) and 26°C (thermoneutral; TN), on the circadian rhythms in mice. We found that the rhythmicity of food intake showed an advanced phase at TC, while the activity was more robust at TN, with a prolonged period onset. The serum levels of norepinephrine were remarkably induced at TC, but failed to oscillate rhythmically at both temperatures. Likewise, circulating glucose levels were increased but were non-rhythmic under TC. Both total cholesterol and triglycerides levels were induced at TN, but showed an advanced phase under TC. Additionally, the expression of hepatic metabolic genes and clock genes remained rhythmic at both temperatures, with the exception of G6Pase, Fasn, Cpt1a and Cry2, at TN. Nevertheless, the liver histology examination did not show any significant changes in response to housing temperature. Although the non-consistent trends of phase changes in each temperature, our results suggest a non-reductant role of temperature in mouse internal rhythmicity resetting. Thus, the temperature-controlled internal circadian synchronization within organs should be taken into consideration when optimizing housing temperature for mice.
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Alexander, Matthew, Kathleen Kokolus, Amanda Costa, Eleanor Clancy-Thompson, Elizabeth Repasky, and David Mullins. "Chronic cold-stress suppresses chemokine production and CD8+ T cell infiltration in the tumor microenvironment (TUM7P.1024)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 142.13. http://dx.doi.org/10.4049/jimmunol.194.supp.142.13.

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Abstract Recently it was reported that maintenance of mice at thermoneutral temperatures (TT, the temperature at which basal metabolism is sufficient to maintain body temperature, 30oC) enhanced antitumor immune responses and reduced tumor growth, relative to standard vivarium temperatures (ST, 22oC). We hypothesized that mice maintained at ST may have impaired production of T cell chemoattractant cytokines and subsequent T cell infiltration. In mice bearing breast tumors or solid or metastatic-like melanomas, intratumoral expression of CXCL9 and CXCL10 (CXCR3-cognate chemokines) was enhanced by maintenance of hosts in TT conditions. Further, tumors of TT-housed mice contained increased numbers of CD8+ T cells. We further hypothesized that the effect of temperature on T cell chemokine pathways may be a result of chronic cold stress, which may induce norepinephrine (NE) production and subsequent activation of β-adrenergic signaling pathways. We observed that pharmacologic blockade of β-adrenergic receptors in mice bearing solid or metastatic-like melanomas recapitulated the increased intratumoral expression of CXCL9 and CXCL10 and increased CD8+ T cell numbers. Because melanoma cells express β-adrenergic receptors, we suggest that chronic cold stress may induce systemic NE production, leading to tumor local activation of receptors and inhibition of tumor-derived chemokine production. These studies suggest potential interventions to improve existing T cell-based immunotherapies.
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36

Li, Xunde, Edward R. Atwill, Lissa A. Dunbar, and Kenneth W. Tate. "Effect of Daily Temperature Fluctuation during the Cool Season on the Infectivity of Cryptosporidium parvum." Applied and Environmental Microbiology 76, no. 4 (December 18, 2009): 989–93. http://dx.doi.org/10.1128/aem.02103-09.

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ABSTRACT The present work calculated the rate of inactivation of Cryptosporidium parvum oocysts attributable to daily oscillations of low ambient temperatures. The relationship between air temperature and the internal temperature of bovine feces on commercial operations was measured, and three representative 24-h thermal regimens in the ∼15°C, ∼25°C, and ∼35°C ranges were chosen and emulated using a thermocycler. C. parvum oocysts suspended in deionized water were exposed to the temperature cycles, and their infectivity in mice was tested. Oral inoculation of 103 treated oocysts per neonatal BALB/c mouse (∼14 times the 50% infective dose) resulted in time- and temperature-dependent reductions in the proportion of infected mice. Oocysts were completely noninfectious after 14 24-h cycles with the 30°C regimen and after 70 24-h cycles with the 20°C regimen. In contrast, oocysts remained infectious after 90 24-h cycles with the 10°C regimens. The estimated numbers of days needed for a 1-log10 reduction in C. parvum oocyst infectivity were 4.9, 28.7, and 71.5 days for the 30, 20, and 10°C thermal regimens, respectively. The loss of infectivity of oocysts induced by these thermal regimens was due in part to partial or complete in vitro excystation.
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Korani, Mitra, Sara Nikoofal-Sahlabadi, Amin R. Nikpoor, Solmaz Ghaffari, Hossein Attar, Mohammad Mashreghi, and Mahmoud R. Jaafari. "The Effect of Phase Transition Temperature on Therapeutic Efficacy of Liposomal Bortezomib." Anti-Cancer Agents in Medicinal Chemistry 20, no. 6 (June 14, 2020): 700–708. http://dx.doi.org/10.2174/1871520620666200101150640.

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Aims: Here, three liposomal formulations of DPPC/DPPG/Chol/DSPE-mPEG2000 (F1), DPPC/DPPG/Chol (F2) and HSPC/DPPG/Chol/DSPE-mPEG2000 (F3) encapsulating BTZ were prepared and characterized in terms of their size, surface charge, drug loading, and release profile. Mannitol was used as a trapping agent to entrap the BTZ inside the liposomal core. The cytotoxicity and anti-tumor activity of formulations were investigated in vitro and in vivo in mice bearing tumor. Background: Bortezomib (BTZ) is an FDA approved proteasome inhibitor for the treatment of mantle cell lymphoma and multiple myeloma. The low solubility of BTZ has been responsible for the several side effects and low therapeutic efficacy of the drug. Encapsulating BTZ in a nano drug delivery system; helps overcome such issues. Among NDDSs, liposomes are promising diagnostic and therapeutic delivery vehicles in cancer treatment. Objective: Evaluating anti-tumor activity of bortezomib liposomal formulations. Methods: Data prompted us to design and develop three different liposomal formulations of BTZ based on Tm parameter, which determines liposomal stiffness. DPPC (Tm 41°C) and HSPC (Tm 55°C) lipids were chosen as variables associated with liposome rigidity. In vitro cytotoxicity assay was then carried out for the three designed liposomal formulations on C26 and B16F0, which are the colon and melanoma cancer mouse-cell lines, respectively. NIH 3T3 mouse embryonic fibroblast cell line was also used as a normal cell line. The therapeutic efficacy of these formulations was further assessed in mice tumor models. Result: MBTZ were successfully encapsulated into all the three liposomal formulations with a high entrapment efficacy of 60, 64, and 84% for F1, F2, and F3, respectively. The findings showed that liposomes mean particle diameter ranged from 103.4 to 146.8nm. In vitro cytotoxicity studies showed that liposomal-BTZ formulations had higher IC50 value in comparison to free BTZ. F2-liposomes with DPPC, having lower Tm of 41°C, showed much higher anti-tumor efficacy in mice models of C26 and B16F0 tumors compared to F3-HSPC liposomes with a Tm of 55°C. F2 formulation also enhanced mice survival compared with untreated groups, either in BALB/c or in C57BL/6 mice. Conclusion: Our findings indicated that F2-DPPC-liposomal formulations prepared with Tm close to body temperature seem to be effective in reducing the side effects and increasing the therapeutic efficacy of BTZ and merits further investigation.
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Park, Eun-Young, Mi-Hwi Kim, Eung-Hwi Kim, Eun-Kyu Lee, In-Sun Park, Duck-Choon Yang, and Hee-Sook Jun. "Efficacy Comparison of Korean Ginseng and American Ginseng on Body Temperature and Metabolic Parameters." American Journal of Chinese Medicine 42, no. 01 (January 2014): 173–87. http://dx.doi.org/10.1142/s0192415x14500128.

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Ginseng has beneficial effects in cancer, diabetes and aging. There are two main varieties of ginseng: Panax ginseng (Korean ginseng) and Panax quinquefolius (American ginseng). There are anecdotal reports that American ginseng helps reduce body temperature, whereas Korean ginseng improves blood circulation and increases body temperature; however, their respective effects on body temperature and metabolic parameters have not been studied. We investigated body temperature and metabolic parameters in mice using a metabolic cage. After administering ginseng extracts acutely (single dose of 1000 mg/kg) or chronically (200 mg/kg/day for four weeks), core body temperature, food intake, oxygen consumption and activity were measured, as well as serum levels of pyrogen-related factors and mRNA expression of metabolic genes. Acute treatment with American ginseng reduced body temperature compared with PBS-treated mice during the night; however, there was no significant effect of ginseng treatment on body temperature after four weeks of treatment. VO 2, VCO 2, food intake, activity and energy expenditure were unchanged after both acute and chronic ginseng treatment compared with PBS treatment. In acutely treated mice, serum thyroxin levels were reduced by red and American ginseng, and the serum prostaglandin E2 level was reduced by American ginseng. In chronically treated mice, red and white ginseng reduced thyroxin levels. We conclude that Korean ginseng does not stimulate metabolism in mice, whereas a high dose of American ginseng may reduce night-time body temperature and pyrogen-related factors.
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Su, Yang-Shuai, Juan-Juan Xin, Zhao-Kun Yang, Wei He, Hong Shi, Xiao-Yu Wang, Ling Hu, Xiang-Hong Jing, and Bing Zhu. "Effects of Different Local Moxibustion-Like Stimuli at Zusanli (ST36) and Zhongwan (CV12) on Gastric Motility and Its Underlying Receptor Mechanism." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/486963.

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The aim of this study was to explore the “intensity-response” relationship in local moxibustion-like stimuli- (LMS-) modulated gastric motility and its underlying receptor mechanism. Based on the thermal pain threshold (43°C), 41°C, 43°C, and 45°C LMS were separately applied to ST36 or CV12 for 180 s among ASIC3 knockout (ASIC3−/−) mice, TRPV1 knockout (TRPV1−/−) mice, and their homologous wild-type C57BL/6 mice (n=8in each group). Gastric motility was continuously measured by an intrapyloric balloon, and the amplitude, integral, and frequency of gastric motility during LMS were compared with those of initial activities. We found that both 43°C and 45°C LMS at ST36 induced significantly facilitated effect of gastric motilityP<0.05, while LMS at CV12 induced inhibited effectsP<0.05. 41°C LMS had no significant impact on gastric motility. Compared with C57BL/6 mice, the facilitatory effect at ST36 and inhibitive effect of LMS at CV12 were decreased significantly in TRPV1−/− mice (P<0.05;P<0.01) but not changed markedly in ASIC3−/− miceP>0.05. These results suggest that there existed an “intensity-response” relationship between temperature in LMS and its effects on gastric motility. TRPV1 receptor played a crucial role in the LMS-modulated gastric motility.
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Chen, Hubert C., Zuleika Ladha, Steven J. Smith, and Robert V. Farese. "Analysis of energy expenditure at different ambient temperatures in mice lacking DGAT1." American Journal of Physiology-Endocrinology and Metabolism 284, no. 1 (January 1, 2003): E213—E218. http://dx.doi.org/10.1152/ajpendo.00248.2002.

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Mice lacking acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1), a key enzyme in triglyceride synthesis, have increased energy expenditure and therefore are resistant to obesity. Because ambient temperature can significantly affect energy expenditure in mice, we undertook these studies to determine the effects of different ambient temperatures on energy expenditure, food intake, and thermoregulation in DGAT1-deficient [ Dgat1(−/−)] mice. Dgat1(−/−) mice had increased energy expenditure irrespective of changes in the ambient temperature. Although core temperature was normal, surface temperature was increased in Dgat1(−/−) mice, most likely reflecting an active mechanism to dissipate heat from increased thermogenesis. Dgat1(−/−) mice had increased food intake at baseline, and this hyperphagia became more pronounced upon exposure to cold. When fasted in a cold environment, Dgat1(−/−) mice developed hypothermia, which was associated with hypoglycemia. These results suggest that the hyperphagia in Dgat1(−/−) mice is a secondary mechanism that compensates for the increased utilization of fuel substrates. Our findings offer insights into the mechanisms of hyperphagia and increased energy expenditure in a murine model of obesity resistance.
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Muzzi, Mirko, Francesco Blasi, Alessio Masi, Elisabetta Coppi, Chiara Traini, Roberta Felici, Maria Pittelli, et al. "Neurological Basis of AMP-Dependent Thermoregulation and its Relevance to Central and Peripheral Hyperthermia." Journal of Cerebral Blood Flow & Metabolism 33, no. 2 (October 24, 2012): 183–90. http://dx.doi.org/10.1038/jcbfm.2012.157.

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Therapeutic hypothermia is of relevance to treatment of increased body temperature and brain injury, but drugs inducing selective, rapid, and safe cooling in humans are not available. Here, we show that injections of adenosine 5′-monophosphate (AMP), an endogenous nucleotide, promptly triggers hypothermia in mice by directly activating adenosine A1 receptors (A1R) within the preoptic area (POA) of the hypothalamus. Inhibition of constitutive degradation of brain extracellular AMP by targeting ecto 5′-nucleotidase, also suffices to prompt hypothermia in rodents. Accordingly, sensitivity of mice and rats to the hypothermic effect of AMP is inversely related to their hypothalamic 5′-nucleotidase activity. Single-cell electrophysiological recording indicates that AMP reduces spontaneous firing activity of temperature-insensitive neurons of the mouse POA, thereby retuning the hypothalamic thermoregulatory set point towards lower temperatures. Adenosine 5′-monophosphate also suppresses prostaglandin E2-induced fever in mice, having no effects on peripheral hyperthermia triggered by dioxymetamphetamine (ecstasy) overdose. Together, data disclose the role of AMP, 5′-nucleotidase, and A1R in hypothalamic thermoregulation, as well and their therapeutic relevance to treatment of febrile illness.
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42

Yang, Jiang-Ning, Jiang-Fan Chen, and Bertil B. Fredholm. "Physiological roles of A1 and A2A adenosine receptors in regulating heart rate, body temperature, and locomotion as revealed using knockout mice and caffeine." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 4 (April 2009): H1141—H1149. http://dx.doi.org/10.1152/ajpheart.00754.2008.

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Heart rate (HR), body temperature (Temp), locomotor activity (LA), and oxygen consumption (O2C) were studied in awake mice lacking one or both of the adenosine A1 or A2A receptors (A1R or A2AR, respectively) using telemetry and respirometry, before and after caffeine administration. All parameters were lower during day than night and higher in females than males. When compared with wild-type (WT) littermates, HR was higher in male A1R knockout (A1RKO) mice but lower in A2ARKO mice and intermediate in A1-A2AR double KO mice. A single dose of an unselective β-blocker (timolol; 1 mg/kg) abolished the HR differences between these genotypes. Deletion of A1Rs had little effect on Temp, whereas deletion of A2ARs increased it in females and decreased it in males. A1-A2ARKO mice had lower Temp than WT mice. LA was unaltered in A1RKO mice and lower in A2ARKO and A1-A2ARKO mice than in WT mice. Caffeine injection increased LA but only in mice expressing A2AR. Caffeine ingestion also increased LA in an A2AR-dependent manner in male mice. Caffeine ingestion significantly increased O2C in WT mice, but less in the different KO mice. Injection of 30 mg/kg caffeine decreased Temp, especially in KO mice, and hence in a manner unrelated to A1R or A2AR blockade. Selective A2B antagonism had little or no effect. Thus A1R and A2AR influence HR, Temp, LA, and O2C in mice in a sex-dependent manner, indicating effects of endogenous adenosine. The A2AR plays an important role in the modulation of O2C and LA by acute and chronic caffeine administration. There is also evidence for effects of higher doses of caffeine being independent of both A1R and A2AR.
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Jun, Jonathan C., Mi-Kyung Shin, Qiaoling Yao, Ronald Devera, Shannon Fonti-Bevans, and Vsevolod Y. Polotsky. "Thermoneutrality modifies the impact of hypoxia on lipid metabolism." American Journal of Physiology-Endocrinology and Metabolism 304, no. 4 (February 15, 2013): E424—E435. http://dx.doi.org/10.1152/ajpendo.00515.2012.

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Hypoxia has been shown to rapidly increase triglycerides in mice by decreasing plasma lipoprotein clearance. However, the usual temperature of hypoxic exposure is below thermoneutrality for mice, which may increase thermogenesis and energy requirements, resulting in higher tissue lipid uptake. We hypothesize that decreased lipid clearance and ensuing hyperlipidemia are caused by hypoxic suppression of metabolism at cold temperatures and, therefore, would not occur at thermoneutrality. Twelve-week-old, male C57BL6/J mice were exposed to 6 h of 10% O2 at the usual temperature (22°C) or thermoneutrality (30°C). Acclimation to 22°C increased lipid uptake in the heart, lungs, and brown adipose tissue, resulting in lower plasma triglyceride and cholesterol levels. At this temperature, hypoxia attenuated lipid uptake in most tissues, thereby raising plasma triglycerides and LDL cholesterol. Thermoneutrality decreased tissue lipid uptake, and hypoxia did not cause a further reduction in lipid uptake in any organs. Consequently, hypoxia at thermoneutrality did not affect plasma triglyceride levels. Unexpectedly, plasma HDL cholesterol increased. The effect of hypoxia on white adipose tissue lipolysis was also modified by temperature. Independent of temperature, hypoxia increased heart rate and glucose and decreased activity, body temperature, and glucose sensitivity. Our study underscores the importance of ambient temperature for hypoxia research, especially in studies of lipid metabolism.
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44

Jennings, G., and M. Elia. "Effect of E. coli endotoxin on temperature, oxygen consumption and brown adipose tissue thermogenesis in rats and mice." Bioscience Reports 7, no. 6 (June 1, 1987): 517–23. http://dx.doi.org/10.1007/bf01116509.

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The effects of E. coli endotoxin 0127 B8 on oxygen consumption, temperature, and on the activity of the proton conductance pathway in brown adipose tissue (BAT) were investigated in rats and mice. In rats an increase was observed in rectal and skin temperature, whole body oxygen consumption and GDP binding in BAT. In mice only the rise in rectal and skin temperature were significantly changed by endotoxin administration. These findings suggest that in some species BAT is involved in the production of endotoxin induced fever and increased energy expenditure.
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45

Li Gao, Yinghu Zhao, and Zhaoliang Liu. "Immune Function Effect Analysis with Aspirin Based on Temperature Model Experiment of Mice." Journal of Convergence Information Technology 7, no. 16 (September 30, 2012): 11–18. http://dx.doi.org/10.4156/jcit.vol7.issue16.2.

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46

Cambridge, Naomi, and Emma S. J. Robinson. "Effect of BU98008, an imidazoline1-binding site ligand, on body temperature in mice." European Journal of Pharmacology 519, no. 1-2 (September 2005): 86–90. http://dx.doi.org/10.1016/j.ejphar.2005.07.010.

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47

Jensen, Birgitte, Jay F. Storz, and Angela Fago. "Bohr effect and temperature sensitivity of hemoglobins from highland and lowland deer mice." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 195 (May 2016): 10–14. http://dx.doi.org/10.1016/j.cbpa.2016.01.018.

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48

Jackson, Helen C., Emma Ramsay, and D. J. Nutt. "Effect of the cyclopyrrolones suriclone and RP 59037 on body temperature in mice." European Journal of Pharmacology 216, no. 1 (May 1992): 23–27. http://dx.doi.org/10.1016/0014-2999(92)90204-h.

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49

Wilkinson, D. A., D. R. Burholt, and P. N. Shrivastava. "Hypothermia following whole-body heating of mice: Effect of heating time and temperature." International Journal of Hyperthermia 4, no. 2 (January 1988): 171–82. http://dx.doi.org/10.3109/02656738809029307.

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50

Tove, Samuel B., Rebecca Gooding, and Martin Nyajom. "Effect of Ambient Temperature on the Toxicity of Palmitoyl Glycerol in Weanling Mice." Journal of Nutrition 115, no. 11 (November 1, 1985): 1477–80. http://dx.doi.org/10.1093/jn/115.11.1477.

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